安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
2期
172-176
,共5页
贾强%杨锐%马善峰%刘小粉%吴继锋
賈彊%楊銳%馬善峰%劉小粉%吳繼鋒
가강%양예%마선봉%류소분%오계봉
硫化氢%心肌损伤%糖尿病%凋亡
硫化氫%心肌損傷%糖尿病%凋亡
류화경%심기손상%당뇨병%조망
hydrogen sulfide%myocardium injury%diabetes mellitus%apoptosis
目的观察硫化氢( H2 S)对糖尿病大鼠心肌损伤的保护作用及其抗凋亡机制。方法雄性SD大鼠随机分为正常对照组( NC 组)、糖尿病对照组( DM 组)、硫氢化钠( NaHS)治疗组( NaHS+DM组)和NaHS对照组( NaHS组)。采用链脲佐菌素(STZ)55 mg/kg腹腔注射诱导糖尿病大鼠模型,造模成功8周后行离体心脏灌流,测定左心室动力学指标;电镜观察心肌细胞超微结构改变;采用分光光度法检测心肌组织Caspase-3的活性;RT-PCR检测左心室心尖组织Bcl-2、Bax mRNA的表达。结果与NC组相比,NaHS 组各项指标差异均无统计学意义( P>0.05),而DM组左心室发展压( LVDP)、左心室内压最大上升速率和下降速率(依dp/dtmax)均明显降低(P<0.01);左心室舒张末压(LVEDP)明显增大( P<0.01);心肌纤维断裂,线粒体肿胀,嵴断裂消失;心肌组织Caspase-3的活性明显增加( P<0.01);Bcl-2/Bax mRNA比值降低(P<0.01)。与DM组相比,NaHS+DM组LVDP、依dp/dtmax增加(P<0.05,P<0.01),LVEDP明显降低(P<0.05),心肌超微结构损伤明显改善,Caspase-3活性明显降低( P <0.01), Bcl-2/Bax mRNA 比值升高( P <0.01)。结论H2 S对糖尿病大鼠心肌损伤具有保护作用,其机制可能与抗心肌细胞凋亡途径有关。
目的觀察硫化氫( H2 S)對糖尿病大鼠心肌損傷的保護作用及其抗凋亡機製。方法雄性SD大鼠隨機分為正常對照組( NC 組)、糖尿病對照組( DM 組)、硫氫化鈉( NaHS)治療組( NaHS+DM組)和NaHS對照組( NaHS組)。採用鏈脲佐菌素(STZ)55 mg/kg腹腔註射誘導糖尿病大鼠模型,造模成功8週後行離體心髒灌流,測定左心室動力學指標;電鏡觀察心肌細胞超微結構改變;採用分光光度法檢測心肌組織Caspase-3的活性;RT-PCR檢測左心室心尖組織Bcl-2、Bax mRNA的錶達。結果與NC組相比,NaHS 組各項指標差異均無統計學意義( P>0.05),而DM組左心室髮展壓( LVDP)、左心室內壓最大上升速率和下降速率(依dp/dtmax)均明顯降低(P<0.01);左心室舒張末壓(LVEDP)明顯增大( P<0.01);心肌纖維斷裂,線粒體腫脹,嵴斷裂消失;心肌組織Caspase-3的活性明顯增加( P<0.01);Bcl-2/Bax mRNA比值降低(P<0.01)。與DM組相比,NaHS+DM組LVDP、依dp/dtmax增加(P<0.05,P<0.01),LVEDP明顯降低(P<0.05),心肌超微結構損傷明顯改善,Caspase-3活性明顯降低( P <0.01), Bcl-2/Bax mRNA 比值升高( P <0.01)。結論H2 S對糖尿病大鼠心肌損傷具有保護作用,其機製可能與抗心肌細胞凋亡途徑有關。
목적관찰류화경( H2 S)대당뇨병대서심기손상적보호작용급기항조망궤제。방법웅성SD대서수궤분위정상대조조( NC 조)、당뇨병대조조( DM 조)、류경화납( NaHS)치료조( NaHS+DM조)화NaHS대조조( NaHS조)。채용련뇨좌균소(STZ)55 mg/kg복강주사유도당뇨병대서모형,조모성공8주후행리체심장관류,측정좌심실동역학지표;전경관찰심기세포초미결구개변;채용분광광도법검측심기조직Caspase-3적활성;RT-PCR검측좌심실심첨조직Bcl-2、Bax mRNA적표체。결과여NC조상비,NaHS 조각항지표차이균무통계학의의( P>0.05),이DM조좌심실발전압( LVDP)、좌심실내압최대상승속솔화하강속솔(의dp/dtmax)균명현강저(P<0.01);좌심실서장말압(LVEDP)명현증대( P<0.01);심기섬유단렬,선립체종창,척단렬소실;심기조직Caspase-3적활성명현증가( P<0.01);Bcl-2/Bax mRNA비치강저(P<0.01)。여DM조상비,NaHS+DM조LVDP、의dp/dtmax증가(P<0.05,P<0.01),LVEDP명현강저(P<0.05),심기초미결구손상명현개선,Caspase-3활성명현강저( P <0.01), Bcl-2/Bax mRNA 비치승고( P <0.01)。결론H2 S대당뇨병대서심기손상구유보호작용,기궤제가능여항심기세포조망도경유관。
Objective To investigate the anti-apoptotic effect of hydrogen sulfide ( H2 S) on its cardioprotection in diabetic rats. Methods Thirty-two male SD rats were divided into four groups randomly: normal control group ( NC) , diabetic group ( DM) , NaHS + diabetic group ( NaHS+DM) and NaHS group ( NaHS) . Diabetic rat was induced by injection of streptozotocin at 55 mg/kg intraperitoneally. After 8 weeks, hearts were excised and per-fused on Langendorff apparatus. Left ventricular hemodynamic parameters were measured. The ultrastructures of myocardium were observed using electron microscopy, and the activity of Caspase-3 was analyzed by spectrophoto-metric method. The expressions of Bcl-2 and Bax at mRNA level in the left anterior myocardium were detected u-sing RT-PCR. Results There had no significant differences of all indexes between NC and NaHS groups ( P >0.05) . However, compared with NC group, in diabetic rats, left ventricular developed pressure ( LVDP) , maxi-mal rise/fall rate of left ventricular pressure ( ±dp/dtmax) were decreased (P<0.01), left ventricular end dias-tolic pressure (LVEDP) was increased (P<0.01). The activity of Caspase-3 was increased(P<0.01), while the ratio of Bcl-2/Bax at mRNA level was decreased(P<0.01). The degeneration of myocardiac myofibrillae and ede-ma of mitochondria were shown in diabetic rats. Compared with DM group, the hemodynamic parameters were re-served , and the injury of myocardiac myofibrillae and mitochondria was attentuated when the diabetic rats were trea-ted with NaHS at 14 μmol/(kg·d). Caspase-3 activity was also decreased (P<0.01), and the ratio of Bcl-2/Bax at mRNA level was increased (P<0.01). Conclusion H2S can protect myocardium in diabetic rats, may be related to suppressing the happening of cell apoptosis.